Structural dissection of apicomplexan gliding motility

Malaria, toxoplasmosis, and cryptosporidiosis are caused by apicomplexan parasites, which invade host cells through gliding motility. A fundamental paradox defines this system: how do parasites achieve efficient gliding using the most unstable actin filaments known in eukaryotes? Recent structural advances have begun to resolve this question by revealing spatial mechanisms that compensate for this instability. Cryo-electron microscopy demonstrated how divergent actin isoforms, specialised connectors, and conserved nucleation sites orchestrate a molecular conveyor belt operating with spatial control. Filaments are nucleated apically, channelled via gates, guided along defined tracks, and recycled posteriorly. This continuous and rapid turnover prevents actin accumulation while enabling efficient motility, critical for parasite transmission.